Interaction between oxidative stress and diabetes: a mini-review

Royana Singh, A. Ashish, Arunim Shah, S. Pandey
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引用次数: 6

Abstract

The Diabetes Mellitus (DM) is increasing in incidence and prevalence worldwide, taking the shape of the pandemic proportions, which is expected to increase further over a couple of decades. In 2019, an estimated 9.3% of the population (463 million people), globally had DM. Projection of future DM burden may increase to 10.2% (578 million people) by 2030 and 10.9% (700 million people) by next 25 years (2045). The decrease in immunity in diabetic patients has been a significant concern for physicians and patients alike. The role of mitochondria and it is cellular signaling can elaborate on this problem in depth. Mitochondria is a rich source of reactive oxygen species (ROS) and plays a crucial role in cellular metabolism for energy. They are targets of ROS and many different cellular signals like mitochondrial membrane apoptosis due to hyperglycemia and ROS. The interplay between oxidative stress and diabetes further activated, leading to increased permeability of mitochondrial membrane & apoptosis; this leads to a decrease in immunity in diabetic patients leading to increased mortality and morbidity. Hyperglycemia and ROS major pathways of apoptosis through mitochondrial activation in diabetic patients leading to decreased immunity. They can become drug targets for further intervention of this problem in Diabetic patients. Access
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氧化应激和糖尿病之间的相互作用:一个小回顾
糖尿病(DM)在世界范围内的发病率和流行率正在增加,呈大流行病的形式,预计在几十年内将进一步增加。2019年,全球估计有9.3%的人口(4.63亿人)患有糖尿病。预计到2030年,未来糖尿病负担可能增加到10.2%(5.78亿人),到未来25年(2045年)可能增加到10.9%(7亿人)。糖尿病患者的免疫力下降一直是医生和患者都非常关注的问题。线粒体的作用和它的细胞信号传导可以深入阐述这个问题。线粒体是活性氧(ROS)的丰富来源,在细胞能量代谢中起着至关重要的作用。它们是活性氧和许多不同细胞信号的靶标,如高血糖和活性氧引起的线粒体膜凋亡。氧化应激与糖尿病的相互作用进一步激活,导致线粒体膜通透性增加和细胞凋亡;这导致糖尿病患者免疫力下降,导致死亡率和发病率增加。高血糖和ROS是糖尿病患者通过线粒体激活细胞凋亡的主要途径,导致免疫力下降。它们可以成为进一步干预糖尿病患者这一问题的药物靶点。访问
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